The lifespan of the short-lived killifish could shed new light on the lifespans of humans, according to new research.
The study, which was conducted by researchers at the Scuola Normale Superiore in Pisa, Italy, and the Leibniz Institute of Aging in Jena, Germany, could also lead to new strategies for treating age-related disease such as type 2 diabetes.
How was the study conducted?
The researchers hypothesised that the African turquoise killifish – the vertebrate with the shortest lifespan – could provide new information on the relationship between gene expression and age-related diseases.
To find out, they divided the fins of killifish into different groups, based on their longevity. At most, killifish live for 12 months, but around four months is more common. In the killifish who lived for the longest, the genes that are responsible for cellular respiration (which occurs when mitochondria within cells use oxygen to burn sugar) were less active at a young age.
Next, the researchers exposed the fish to a low dose of rotenone, a natural poison that inhibits the proteins that trigger cellular respiration. The killifish lived longer as a result.
It is not guaranteed that the findings will be replicated in humans, although the researchers have reason to be hopeful: both killifish and humans lose mitochondria function as they get older, and this research contradicts previous assumptions that improving mitochondrial function would make older people healthier.
“Up to the present, it was thought that improving mitochondrial function would improve health in aged people; however, our results indicate a more complex scenario where the partial inhibition of mitochondrial function paradoxically has beneficial effects,” said Alessandro Cellerino, of the Scuola Normale Superiore in Pisa, Italy, and the Leibnez Institute of Aging in Jena, Germany.
Why might this be the case?
It is not entirely understood why slightly decreasing mitochondrial function makes killifish – and potentially humans – live longer, but the researchers suspect it may be down to a mechanism that adapts to stress.
Cellerino explained: “The mechanism of adaptation after stress is called hormesis, and it was recently demonstrated that the positive effects of physical exercise in humans are due to hormesis and are destroyed by treatment with antioxidants.
“This obviously has implications on the development of strategies to improve health in older people and prevent aging-associated diseases.”
The researchers note that there are already approved drugs that slightly inhibit mitochondrial complex I, which this study found can improve health in old age. The popular type 2 diabetes medication metformin is one such drug. A recent study found that metformin can extend the lifespan of mice, and it also inhibits mitochondrial complex I; it’s quite possible that the two things are related.
“Based on our data, we strongly suspect that the effect of metformin was due to inhibition of complex I and not to its anti-diabetic action.”
The findings are published in Cell Systems.

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